The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143

Huang, Fengting; Chen, Wenying; Gu, Zhong Ze; Zhuang, Yanyan; Li, Chu-Qiang; Wang, Lingyun; Peng, Jintao; Zhu, Zhe; Luo, Xin; Li, Yuanhua; Yao, Herui; Zhang, Shineng

doi:10.1038/cddis.2017.191

Cited by 53 publications

(51 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…demonstrated that the lncRNA GAS5 suppresses cell growth and the EMT in osteosarcoma by regulating the miR-221/ ARHI pathway. Huang et al [52]. reported that the novel long intergenic noncoding RNA upregulated in CRC (UCC) promoted CRC progression by sponging miR-143.…”

Section: Discussionmentioning

confidence: 99%

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

show abstract

Section: Discussionmentioning

confidence: 99%

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Currently, accumulating evidence has shown that lncRNAs play a critical role in the pathogenesis of cancer (F.T. Huang, Chen, et al, 2017;Shi et al, 2017;X. Wang, Lu, Geng, Yang, & Shi, 2017;.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA FAM83H‐AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21)

Shen

Quan

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Gliomas are the commonest and most aggressive primary malignant tumor in the central nervous system. Long noncoding RNAs (lncRNAs) have been identified to act as crucial regulators in multiple biological processes, including tumorigenesis. FAM83H antisense RNA1 (FAM83H-AS1) has been uncovered to be dysregulated in several cancers. However, the biological role of FAM83H-AS1 in glioma still needs to be investigated. Currently, our findings indicated that FAM83H-AS1 was upregulated in glioma tissues and cell lines and high level of FAM83H-AS1 was associated with poor prognosis of glioma. Loss-of-function assays demonstrated that silenced FAM83H-AS1 obviously suppressed cell proliferation via regulating the cell-cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation. Collectively, our findings suggested that FAM83H-AS1 participated in the progression of glioma and might act as a potential therapeutic target and prognosis biomarker for human glioma.

show abstract

“…The latest study revealed that lncRNA CRNDE may promote CRC cell proliferation and chemoresistance by modulating miR‐181a‐5p and the Wnt/β‐catenin signalling pathway . In addition, a novel lincRNA termed “UCC” was found to be highly expressed in human CRC tissues and cell lines and to facilitate CRC progression by acting as a sponge for miR‐143 . The expression of lnc‐sox5 is significantly higher in CRC and regulates CRC tumourigenesis by unbalancing the tumour microenvironment .…”

Section: Introductionmentioning

confidence: 99%

“…7 In addition, a novel lincRNA termed "UCC" was found to be highly expressed in human CRC tissues and cell lines and to facilitate CRC progression by acting as a sponge for miR-143. 8 The expression of lnc-sox5 is significantly higher in CRC and regulates CRC tumourigenesis by unbalancing the tumour microenvironment. 9 A long intergenic non-coding RNA called LINC00312, encoded in chromosomal region 3p25.3, has been reported to be a novel tumour suppressor gene in several cancers, [10][11][12] but its role and mechanism of action in CRC development remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

LINC00312 represses proliferation and metastasis of colorectal cancer cells by regulation of miR‐21

Wang

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

Long non‐coding RNAs (lncRNAs) have emerged as important regulators of cancer, including colorectal cancer (CRC). The exact expression pattern of long intergenic noncoding RNA 00312 (LINC00312) in CRC and its mechanisms of action have not been reported. Here, we found that LINC00312 is underexpressed in CRC tissues and cell lines. Functional experiments suggested that LINC00312 suppresses growth, migration and invasion of CRC cells in vitro and attenuates tumour proliferation and metastasis in vivo. Mechanistically, LINC00312 was found to regulate the malignancy of CRC cells by binding to miR‐21 and by functioning as a tumour suppressor targeting PTEN. Overexpression of miR‐21 or knockdown of PTEN attenuated the LINC00312‐mediated inhibition of CRC cell proliferation and invasion. Taken together, our results elucidate the role of the LINC00312–miR‐21–PTEN axis in CRC cell proliferation and tumour progression and may lead to new lncRNA‐based diagnostics or therapeutics for CRC.

show abstract

The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143

Cited by 53 publications

References 48 publications

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Long noncoding RNA FAM83H‐AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21)

LINC00312 represses proliferation and metastasis of colorectal cancer cells by regulation of miR‐21

Contact Info

Product

Resources

About